Abstract
Introduction: Impaired glucose tolerance is common in COPD [Archer & Baker, Resp Med: COPD Update 2009;5:67-74]. We assessed pancreatic function, hepatic and peripheral insulin resistance and determined the relationship of these with systemic inflammation.
Methods: Participants were 8 stable COPD patients (C) (4 male, 66±8yrs, FEV1 44±16%predicted, body mass index (BMI) 23±6kg/m2) and 8 healthy volunteers (V) (8m, 24±5yrs, FEV1 89±12%, BMI 22±2kg/m2) without diabetes mellitus and with fasting glucose <7mM. Participants underwent 120min oral glucose tolerance testing (OGTT). Hepatic insulin resistance (HOMA2-IR) and pancreatic beta-cell function (HOMA2-%B) were derived from fasting values and the Matsuda Index (composite hepatic and muscle insulin sensitivity) from OGTT values.
Results: Fasting glucose (p=0.038), HbA1C (p=0.013) and C peptide (p=0.028) were higher in COPD than in volunteers, but insulin was not different (p=0.234). HOMA2-%B was: C 126 [81-182], V 91 [86-113], p=0.279, HOMA2-IR was: C 1.3 [0.8-1.8], V 1.0 [0.7-1.2], p=0.161, Matsuda Index was: C 3 [3-5], V (8 [6-10], p=0.002. In COPD, but not volunteers, ln(CRP) was inversely correlated with ln(Matsuda) (R=-0.760, p=0.047) but not with other homeostatic measures after controlling for BMI.
Conclusion: Non-obese COPD patients without diabetes had increased composite, but not hepatic, insulin resistance compared to volunteers, indicating skeletal muscle insulin resistance. Possible mechanisms underlying the correlation between peripheral insulin resistance and inflammation include inhibition of insulin receptor signalling by inflammatory mediators or pro-inflammatory effects of elevated glucose.
- © 2011 ERS